title: Thymic stroma-derived T cell growth factor (TSTGF): III. Its ability to promote T cell proliferation without stimulating interleukin 2- or 4-dependent autocrine mechanism.
abstract: A thymic stroma-derived cell clone, MRL104.8a produced a T cell growth factor designated as thymic stroma-derived T cell growth factor (TSTGF). This factor that is distinct from previously described T cell growth factors such as interleukin (IL) 2 or 4 was capable of promoting the growth of IL2-dependent, antigen-specific helper T cell clones. While such growth promotion was induced without requirement of the relevant antigen and exogenous IL2, we further investigated whether it depended on activation of an IL2- or IL4-dependent autocrine mechanism. Helper T cell clones, 8-E and 8-5, were able to proliferate in response to stimulation with either antigen or TSTGF. 8-E and 8-5 produced IL2 and IL4, respectively, in cultures following antigenic stimulation, whereas neither IL2 nor IL4 activity was detected in cultures during TSTGF-induced proliferation. The proliferation of these helper T cell clones by antigenic stimulation was almost completely inhibited when anti-IL2 receptor or anti-IL4 antibody was added to the cultures. The addition of cyclosporin A (CsA) to cultures of 8-E and 8-5 clones together with antigen also resulted in the complete inhibition of cellular proliferation in association with the suppression of IL2 and IL4 production. In contrast, TSTGF-induced proliferation was not affected by addition of either type of antibody or CsA. These results indicate that TSTGF is a novel T cell growth factor that can exert its own growth-promoting effect without depending on an IL2- or IL4-operating autocrine mechanism.
authors.affiliation: Biomedical Research Center, Osaka University Medical School, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Kosaka
authors.forename: M
authors.initials: M
authors.lastname: Ogata
authors.forename: H
authors.initials: H
authors.lastname: Sano
authors.forename: S
authors.initials: S
authors.lastname: Sakuma
authors.forename: Y
authors.initials: Y
authors.lastname: Mizushima
authors.forename: E
authors.initials: E
authors.lastname: Nakamura
authors.forename: H
authors.initials: H
authors.lastname: Teraoka
authors.forename: T
authors.initials: T
authors.lastname: Hamaoka
authors.forename: H
authors.initials: H
authors.lastname: Fujiwara
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D003524:Cyclosporins / Q000494:pharmacology; D007376:Interleukin-2 / Q000276:immunology / Q000378:metabolism / Q000494:pharmacology* / Q000502:physiology; D015847:Interleukin-4 / Q000276:immunology / Q000378:metabolism / Q000502:physiology; D013950:Thymus Gland / Q000166:cytology / Q000378:metabolism*
chemical_list: D000911:Antibodies, Monoclonal; D003524:Cyclosporins; D007376:Interleukin-2; D015847:Interleukin-4